TY - JOUR
T1 - Activin type IB receptor signaling in prostate cancer cells promotes lymph node metastasis in a xenograft model
AU - Nomura, Masatoshi
AU - Tanaka, Kimitaka
AU - Wang, Lixiang
AU - Goto, Yutaka
AU - Mukasa, Chizu
AU - Ashida, Kenji
AU - Takayanagi, Ryoichi
N1 - Funding Information:
We thank Dr. Kohei Miyazono, Joan Massague, and Lawrence S. Mathews for kindly donating the plasmids. We also thank Dr. Shuli Fan and Ms. Akiko Nakano for their technical assistance. This work was supported in part by JSPS KAKENHI Grant Number 23591356 (MN), Grants-in-Aid for JSPS postdoctoral fellowship for foreign researchers (LW). The work of M.N. was supported by grant from Medical Research Encouragement Prize of The Japan Medical Association .
PY - 2013/1/4
Y1 - 2013/1/4
N2 - Activin, a member of the transforming growth factor-β family, has been known to be a growth and differentiating factor. Despite its pluripotent effects, the roles of activin signaling in prostate cancer pathogenesis are still unclear. In this study, we established several cell lines that express a constitutive active form of activin type IB receptor (ActRIBCA) in human prostate cancer cells, ALVA41 (ALVA-ActRIBCA). There was no apparent change in the proliferation of ALVA-ActRIBCA cells in vitro; however, their migratory ability was significantly enhanced. In a xenograft model, histological analysis revealed that the expression of Snail, a cell-adhesion-suppressing transcription factor, was dramatically increased in ALVA-ActRIBCA tumors, indicating epithelial mesenchymal transition (EMT). Finally, mice bearing ALVA-ActRIBCA cells developed multiple lymph node metastases. In this study, we demonstrated that ActRIBCA signaling can promote cell migration in prostate cancer cells via a network of signaling molecules that work together to trigger the process of EMT, and thereby aid in the aggressiveness and progression of prostate cancers.
AB - Activin, a member of the transforming growth factor-β family, has been known to be a growth and differentiating factor. Despite its pluripotent effects, the roles of activin signaling in prostate cancer pathogenesis are still unclear. In this study, we established several cell lines that express a constitutive active form of activin type IB receptor (ActRIBCA) in human prostate cancer cells, ALVA41 (ALVA-ActRIBCA). There was no apparent change in the proliferation of ALVA-ActRIBCA cells in vitro; however, their migratory ability was significantly enhanced. In a xenograft model, histological analysis revealed that the expression of Snail, a cell-adhesion-suppressing transcription factor, was dramatically increased in ALVA-ActRIBCA tumors, indicating epithelial mesenchymal transition (EMT). Finally, mice bearing ALVA-ActRIBCA cells developed multiple lymph node metastases. In this study, we demonstrated that ActRIBCA signaling can promote cell migration in prostate cancer cells via a network of signaling molecules that work together to trigger the process of EMT, and thereby aid in the aggressiveness and progression of prostate cancers.
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U2 - 10.1016/j.bbrc.2012.11.011
DO - 10.1016/j.bbrc.2012.11.011
M3 - Article
C2 - 23159635
AN - SCOPUS:84872418296
SN - 0006-291X
VL - 430
SP - 340
EP - 346
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -
